This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The primary goal of this research is to further our understanding of the neurobiological basis of social bonding, using a unique non-human primate model. Dysfunctions in social bonding underlie a number of developmental and psychiatric disorders, as well as having long-term consequences for physical and psychological health. In this broader context, we propose to study a species which displays high levels of selective social bonding, the monogamous titi monkey (Callicebus cupreus). This species displays a pair-bond, or selective attachment between males and females, as well as attachment by offspring to their father. Non-human primate models are a valuable addition to rodent models, in being neuroanatomically much closer to humans. In many cases they are also preferable to studying humans directly, because of the greater control possible over individual experience and experimental conditions. Arginine vasopressin (AVP) and oxytocin (OT) are neuropeptide hormones known to be involved in social bonding in rodents. Although there is also evidence for their role in primate social bonding, the directionality of the process is unclear. We propose to distinguish between three models of the relationship between AVP, OT and social bonding: a) Maturational - the formation of social bonds in a monogamous species are the results of irreversible, age-related maturational processes in which changes in the AVP and OT systems (increases in synthesis, changes in receptor binding) set up a predisposition to form a pair-bond;b) Situational - changes in the AVP and OT systems are completely environmental and the direct result of the formation of a pair-bond or parental attachment. In this model, these changes are reversible upon the loss of the attachment figure, and c) Combination - while irreversible maturational changes in AVP and/or OT set the stage for formation of an adult attachment, the formation of a pair-bond then induces further changes and the loss of an attachment figure can "reset" the process. Our previous research in this species shows evidence for both maturational changes (gonadal hormones, Valeggia et al., 1999) and situational changes (adrenocortical response to formation and disruption of attachment bonds, Mendoza et al., 2000). Our overarching hypothesis for the current research is that both processes are combined with respect to neuropeptide regulation of pair-bonding - the proposed "combination" model.